This invention relates to a novel method for the in vivo paving of the interior of organs or organ components and other tissue cavities, and to apparatus and polymeric products for use in this method. The tissues involved may be those organs or structures having hollow or tubular geometry, for example blood vessels such as arteries or veins, in which case the polymeric products are deposited within the naturally occurring lumen. Alternatively, the tissue may be a normally solid organ in which a cavity has been created either as a result of a surgical procedure, a percutaneous intervention, an accidental trauma, or disease.
The hollow or tubular geometry of organs commonly has functional significance such as in the facilitation of fluid or gas transport (blood, urine, lymph, oxygen or respiratory gasses) or cellular containment (ova, sperm). Disease processes may affect organ tissue or its components by encroaching upon, obstructing or otherwise reducing the cross-sectional area of the hollow or tubular elements. Additionally, other disease processes may violate the native boundaries of the hollow organ and thereby affect its barrier function and/or containment ability. The ability of the organ or structure to properly function can then be severely compromised. A good example of this phenomena can be seen in the coronary arteries.
Coronary arteries, or arteries of the heart, perfuse the cardiac muscle with arterial blood. They also provide essential nutrients, removal of metabolic wastes, and gas exchange. These arteries are subject to relentless service demands for continuous blood flow throughout the life of the patient.
Despite their critical life supporting function, coronary arteries are often subject to attack through several disease processes, the most notable being atherosclerosis (hardening of the arteries). Throughout the life of the patient, multiple factors contribute to the development of microscopic and/or macroscopic vascular lesions known as plaques.
The development of a plaque-lined vessel typically leads to an irregular inner vascular surface with a corresponding reduction of lumen cross-sectional area. The progressive reduction in cross-sectional area compromises flow through the vessel. In the case of the coronary arteries, the result is a reduction in blood flow to the cardiac muscle. This reduction in blood flow, coupled with a corresponding reduction in nutrient and oxygen supply, often results in clinical angina, unstable angina, myocardial infarction (heart attack), and death. The clinical consequences of the above process and its overall importance are evidenced by the fact that atherosclerotic coronary artery disease represents the leading cause of death in the United States today.
Historically, for coronary artery disease states beyond those which can be treated solely with medication, the treatment of advanced atherosclerotic coronary artery disease involved cardio-thoracic surgery in the form of coronary artery bypass grafting (CABG). In that procedure, the patient is placed on cardio-pulmonary bypass and the heart muscle is temporarily stopped. Repairs are then surgically affected on the heart in the form of detour conduit grafted vessels to provide blood flow around obstructions. While CABG has proven to be quite effective, it carries with it inherent surgical risks and requires a lengthy, often painful recuperation period. In the United States alone approximately 150,000-200,000 people are subjected to open heart surgery annually.
In 1977 a major advance in the treatment of atherosclerotic coronary artery disease occurred with the introduction of a technique known as Percutaneous Transluminal Coronary Angioplasty (PTCA). PTCA involves the retrograde introduction, typically from an artery in the arm or leg to the area of vessel occlusion, of a catheter with a small dilating balloon at its tip. The catheter is guided through the arteries via direct fluoroscopic guidance and passed across the luminal narrowing of the vessel. Once in place, the catheter balloon is inflated to several atmospheres of pressure. This results in "cracking", "plastic" or other mechanical deformation of the lesion or vessel with a subsequent increase in the cross-sectional area through the lesion. This in turn reduces obstruction and trans-lesional pressure gradients and increases blood flow.
PTCA is an extremely effective treatment with a relatively low morbidity. The procedure has rapidly become the primary therapy in the treatment of advanced atherosclerotic coronary disease throughout the United States and the world. By way of example, since its introduction in 1977, the number of PTCA cases now exceeds 300,000 per annum in the United States and in 1987, for the first time surpassed the number of bypass operations performed. Moreover, as a result of PTCA, emergency coronary artery bypass surgery is required in less than four percent of patients.
Typically, atherosclerosis is a diffuse arterial disease process exhibiting simultaneous patchy involvement in several coronary arteries. Patients with this type of widespread coronary involvement, while previously not considered candidates for angioplasty, are now being treated due to technical advances and increased clinical experience.
Despite the major therapeutic advance in the treatment of coronary artery disease which PTCA represents, its success has been hampered by the development of vessel renarrowing or reclosure following dilation. During a period of hours or days post procedure, significant total vessel reclosure may develop in up to 10% of cases. This occurrence is referred to as "abrupt reclosure". However, the more common and major limitation of PTCA, is the development of progressive reversion of the vessel to its closed condition, negating any gains achieved from the procedure.
This more gradual renarrowing process is referred to as "restenosis" Post-PTCA follow-up studies report a 10-50% incidence (averaging approximately 30%) of restenosis in cases of initially successful angioplasty. Studies of the time course of restenosis have shown that it is typically an early phenomenon, occurring almost exclusively within the six months following an angioplasty procedure. Beyond this six-month period, the incidence of restenosis is quite rare. Despite recent pharmacologic and procedural advances, little success has been achieved in preventing either abrupt reclosure or restenosis post-angioplasty.
Restenosis has become even more significant with the increasing use of multi-vessel PTCA to treat complex coronary artery disease. Studies of restenosis in cases of multi-vessel PTCA reveal that after multi-lesion dilatation, the risk of developing at least one recurrent coronary lesion ranges from about 26% to 54% and appears to be greater than that reported for single vessel PTCA. Moreover, the incidence of restenosis increases in parallel with the severity of the pre-angioplasty vessel narrowing. This is significant in light of the growing use of PTCA to treat increasingly complex multi-vessel coronary artery disease.
The 30% overall average restenosis rate has significant costs including patient morbidity and risks as well as medical economic costs in terms of follow-up medical care, repeat hospitalization and recurrent catherization and angioplasty procedures. Most significantly, prior to recent developments, recurrent restenosis following multiple repeat angioplasty attempts could only be rectified through cardiac surgery with the inherent risks noted above.
In 1987, a mechanical approach to human coronary artery restenosis was introduced. That approach is commonly referred to as "Intracoronary Stenting". One type of intracoronary stent is a tubular device made of fine wire mesh, typically stainless steel. A stent of that type is disclosed in U.S. Pat. No. 4,655,771. The device can be radially compressed so as to be of low cross-sectional area. In this "low profile" condition, the mesh is placed in or on a catheter similar to those used for PTCA. The stent is then positioned at the site of the vascular region to be treated. Once in position, the wire mesh stent is released and allowed to expand to its desired cross-sectional area generally corresponding to the internal diameter of the vessel. Similar solid stents are also disclosed in U.S. Pat. No. 3,868,956 to Alfidi et al.
The metal stent functions as a permanent intra-vascular scaffold. By virtue of its material properties, the metal stent provides structural stability and direct mechanical support to the vascular wall. Stents of the type described above are resiliently self-expanding due to their helical "spring" geometry. Recently, slotted steel tubes and extended spring designs have been introduced. These are deployed through application of direct radial mechanical pressure conveyed by a balloon or other radial expansion device at the catheter tip. Such a device and procedure are disclosed in U.S. Pat. No. 4,733,665 to Palmaz. Despite certain significant limitations and potentially serious complications (discussed below), this type of stent has been successful with an almost 100% acute patency rate and a marked reduction in the restenosis rate.
Other stents have also been designed in recent years. Among these are stents formed from polymeric materials and stents formed from materials which exhibit shape memory. In the latter case, stents formed from the shape memory alloy Nitinol have been disclosed in the prior art.
The complications associated with permanent implants such as the Palmaz device result from both the choice of material, as well as the inherent design deficiencies in the stenting devices. The major limitation lies in the permanent placement of a non-retrivable, non-degradable, foreign body in a vessel to combat restenosis which is predominately limited to the six-month time period post-angioplasty. There are inherent, significant risks common to all permanent implant devices. Moreover, recent studies have revealed that atrophy of the media, the middle arterial layer of a vessel, may occur as a specific complication associated with metal or other permanent stenting due to the application of continuous lateral expansile forces after implantation.
These problems are even more acute in the placement of a permanent metallic foreign body in the vasculature associated with the cardiac muscle. Coronary arteries are subjected to extreme service demands requiring continuous unobstructed patency with unimpeded flow throughout the life of the patient. Failure in this system can lead to myocardial infarction (heart attack) and death. In addition, torsional and other multi-directional stresses encountered in and near the heart, due to its continuous oscillatory/cyclic motion, further amplify the risks associated with permanent, stiff intra-arterial implants in the coronary region.
It has been observed that, on occasion, recurrent intravascular narrowing has occurred following stent placement in vessels during a period of several weeks to months. Typically, this occurs "peri-stent", i.e., immediately upstream or downstream from the stent. It has been suggested that this may relate to the often significantly different compliances of the vessel and the stent, sometimes referred to as "compliance mismatch". Aside from changes in compliance, another important mechanism leading to luminal narrowing above and below the stent may be the changes in shear forces and fluid flows encountered across the sharp transitions of the stent-vessel interface. Further supporting evidence has resulted from studies of vascular grafts which reveal a higher incidence of thrombosis and eventual luminal closure also associated with significant compliance mismatch.
To date, known stent designs, (i.e., tubular, wire helical or spring, and scaffold) have been designed with little consideration or measurement of their radial stiffness. Recent studies measuring the relative radial compressive stiffness of known wire stents, as compared to physiologically pressurized arteries, have found the stents to be much stiffer than biological tissue. These studies lend support to the concept of poor mechanical biocompatibility of currently available stents.
Conventional metal stenting is also limited since it requires the availability of numerous stents of differing sizes (as well as associated deployment devices) to accommodate treatment of blood vessels of differing sizes. Additionally metal stents provide a relatively rigid nonflexible structural support which is not amenable to a wide variety of endoluminal geometries, complex surfaces, luminal bends, curves or bifurcations.
The identified risks and limitations of metal and non-metal permanent stents have severely limited their utility in coronary artery applications. Thus, a need exists for stents which are non-permanent and have a compliance that more closely matches that of blood vessels. A need also exists for stents which may be tailored in length and radial diameter to properly match a wide variety of treatment sites. A need also exists for methods for providing polymeric materials to various body lumens and hollow spaces, whether occurring naturally or as a result of surgery, trauma or disease.